JURNALL

HHS Public Access
Author manuscript
Nat Rev Nephrol. Author manuscript; available in PMC 2021 March 27.
Author Manuscript
Published in final edited form as:

Nat Rev Nephrol. 2020 April ; 16(4): 223–237. doi:10.1038/s41581-019-0244-2.
The global epidemiology of hypertension

Katherine T Mills, PhD, Andrei Stefanescu, MS, Jiang He, MD, PhD
Department of Epidemiology (KTM, AS and JH), Tulane University School of Public Health and
Tropical Medicine and Tulane University Translational Sciences Institute (KTM and JH), New Orleans,
LA
Abstract
Author Manuscript
Hypertension is the leading cause of cardiovascular disease and premature death worldwide.
Owing to widespread use of antihypertensive medications, global mean blood pressure (BP) has
remained constant or decreased slightly over the past four decades. By contrast, the prevalence
of hypertension has increased, especially in low and middle-income countries (LMICs).
Estimates suggest that in 2010, 31.1% of adults (1.39 billion) worldwide had hypertension. The
prevalence of hypertension among adults was higher in LMICs (31.5%, 1.04 billion people) than
in high- income countries (HICs; 28.5%, 349 million people). Variations in the levels of risk
factors for hypertension, such as high sodium intake, low potassium intake, obesity, alcohol
consumption, physical inactivity and unhealthy diet, may explain some of the regional
heterogeneity in hypertension prevalence. Despite the increasing prevalence, the proportions of
hypertension awareness, treatment and BP control are low, particularly in LMICs, and few
comprehensive assessments of the economic impact of hypertension exist. Future studies are
Author Manuscript
warranted to test implementation strategies for hypertension prevention and control, especially in
low-income populations, and to accurately assess the prevalence and financial burden of
hypertension worldwide.
INTRODUCTION
Hypertension is the leading preventable risk factor for cardiovascular disease (CVD) and
all- cause mortality worldwide.1,2 In 2010, 31.1% of the global adult population (1.39
billion people) had hypertension, defined as systolic BP ≥140 mmHg and/or diastolic BP
≥90 mmHg.3 The prevalence of hypertension is rising globally owing to ageing of the
population and increases in exposure to lifestyle risk factors including unhealthy diets (i.e.
high sodium and low potassium intake and lack of physical activity.3 However, changes in
Author Manuscript
hypertension prevalence are not uniform worldwide. In the past two decades, high-income
countries (HICs) experienced a modest decrease in hypertension prevalence, while low and
middle- income countries (LMICs) experienced significant increases. 3 These disparities in
hypertension prevalence trends suggest that health care systems in LMICs could be facing a
Tele: 504-988-5165;
jhe@tulane.edu.
Competing interest statement
The authors declare no competing interests.
Mills et al. Page 2
rapidly increasing burden of hypertension and BP-related cardiovascular diseases, in

some cases in addition to a substantial burden of infectious diseases.
Author Manuscript
In this Review, we discuss estimates and trends in mean BP levels and hypertension
prevalence, awareness, treatment, and control worldwide. We also examine risk factors for
hypertension, strategies for hypertension control, and evidence of the financial burden of
hypertension. We conclude by discussing the consequences of current trends in
hypertension and areas where more research is needed.
GLOBAL MEAN BLOOD PRESSURE

A study that analyzed data from 844 studies performed in 154 countries with 8.69 million
participants estimated that in 2015, the global mean age-standardized systolic BP was 127.0
mmHg in men and 122.3 mmHg in women, whereas the mean age-standardized diastolic BP
Author Manuscript
was 78.7 mmHg in men and 76.7 mmHg in women.4 Higher mean systolic and diastolic BPs
in both men and women were found in South Asia, Sub-Saharan Africa, and Central and
Eastern Europe, while lower mean BPs were found in high-income Western and high-
income Asia-Pacific regions.4 Social and environmental factors, including healthcare access,
availability of antihypertensive medications, and regional variations in hypertension risk
factors, such as obesity, alcohol consumption, unhealthy diet and lack of physical activity,
likely contribute to these regional differences3,4
This study also reported that over the past 40 years, estimated mean BP has remained
constant or decreased slightly worldwide.4 Estimated global mean age-standardized systolic
BP remained fairly constant in men between 1975 (126.6 mmHg) and 2015 (127.0 mmHg)
but decreased slightly in women during this period (from 123.9 mmHg to 122.3 mmHg).
Trends for men and women were similar for estimated global mean age-standardized
Author Manuscript
diastolic BP, with very little change in men and a slight decrease in women. However,
regional changes in estimated mean BP between 1975 and 2015 were more heterogeneous
(Figure 1). In general, HICs experienced a significant BP decrease, while BP in LMIC
regions increased.4 Substantial decreases in estimated age-standardized mean systolic and
diastolic BP occurred in both men and women in high-income Western and Asia-Pacific
regions between 1975 and 2015.4 Estimates suggest that the largest decrease in systolic BP
was in the high-income Asia-Pacific region in which systolic BP decreased by 2.4 mmHg
per decade in men and 3.2 mmHg per decade in women, whereas the largest decrease in
diastolic BP was in the high-income Western region in which diastolic BP decreased by 1.5
mmHg per decade in men and 1.8 mmHg per decade in women. Decreases in mean systolic
and diastolic BP were also observed in women in Central and Eastern Europe, Latin
America and the Caribbean, the Middle East and North Africa, and Central Asia, while no
Author Manuscript
change in BP was seen in men in these regions.4 In both men and women, systolic and
diastolic BP increased in East and Southeast Asia, South Asia, Oceania, and sub-Saharan
Africa.
These regional changes in mean systolic and diastolic BP have led to disparities in the
burden of hypertension.3 Improvements in prevention, detection, and treatment of BP in
HICs have likely contributed to lower BP levels in these regions.3–7 By contrast, limited
Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

Mills et al. Page 3
healthcare resources together with population ageing and urbanization, which is associated
with reductions in physical activity and increases in unhealthy diets, are potential drivers
Author Manuscript
of BP increases in LMICs.8–10 In both HICs and LMICs, women have higher proportions
of hypertension awareness, treatment, and control than men.3 These differences could
contribute to the greater BP reductions observed in women than men in some regions
GLOBAL BURDEN OF HYPERTENSION

Based on an analysis of data from 135 population-based studies that included 968,419 adults
from 90 countries, we estimated that in 2010 the global age-standardized prevalence of
hypertension (defined as systolic BP ≥140 mm Hg, diastolic BP ≥90 mm Hg, and/or current
use of antihypertensive medication) was 31.1% (95% CI 30.0–32.2%).3 The age-
standardized prevalence of hypertension was slightly higher in men (31.9%) than in women
(30.1%) (Table 1)3 and was lower in HICs (28.5%) than in LMICs (31.5%) (Figure 2).3 The
Author Manuscript
lowest prevalence of hypertension in men was found in South Asia (26.4%), whereas the
highest prevalence was in Eastern Europe and Central Asia (39.0%). In women, the
prevalence of hypertension was lowest in HICs (25.3%) and highest in Sub-Saharan Africa
(36.3%). The reasons for these disparities in hypertension prevalence across regions are not
fully understood but are likely influenced by differences in the prevalence of risk factors for
hypertension, including unhealthy diet, lack of physical activity and obesity.3,8
The Prospective Urban Rural Epidemiology (PURE) study included 153,996 adults aged 35–
70 years from 628 rural and urban communities in 17 geographically and economically
diverse countries who were recruited between 2003 and 2009.11 This study included 142,042
participants with BP data at baseline, providing a unique opportunity to compare
hypertension prevalence between rural and urban populations in different world regions. The
Author Manuscript
PURE study found that 40.8% (95% CI 40.5–41.0%) of participants had hypertension with a
higher prevalence in men (41.4%) than in women (37.7%).11 Residents of rural areas had a
higher prevalence of hypertension than urban residents in HICs and middle-income countries
(MICs), but the opposite was true in low-income countries (LICs).11
We estimated that between 2000 and 2010, the global age-standardized prevalence of
hypertension in adults aged ≥20 years increased by 5.2%.3 This estimate is consistent with a
2015 Global Burden of Disease analysis that found that the prevalence of elevated systolic
BP (≥140 mmHg) increased 3.2% from 17.3% in 1990 to 20.5% in 2015.12 The global
increase in prevalence of hypertension was consistent by sex (5.5% in men and 5.0% in
women) but varied by economic development.3 From 2000 to 2010, the prevalence of
hypertension increased in LMICs and decreased in HICs (Table 1).3 LMICs experienced a
sharp increase in hypertension prevalence from 23.8% in 2000 to 31.5% in 2010. By
Author Manuscript
contrast, HICs experienced a decrease in hypertension prevalence from 31.1% to 28.5% in

the same ten-year period.3 Hypertension prevalence was therefore higher in LMICs (31.5%)
than in HICs (28.5%) in 2010. Similar to the trends observed for BP change, population
ageing, urbanization and related lifestyle changes (such as unhealthy diet and lack of
physical activity) might explain the increased prevalence of hypertension in LMICs.8,10

Mills et al. Page 4
As mentioned above, an estimated 1.39 billion adults worldwide had hypertension in 2010
with an approximately even distribution between men and women (Table 1).3 Among those
Author Manuscript
with hypertension, approximately 75% (1.04 billion) lived in LMICs and 25% (349 million)
lived in HICs. By contrast, in 2000 an estimated 921 million people had hypertension
comprising 322 million (34%) in HICs and 599 million (66%) in LMICs.3,13 Between 2000
and 2010, the absolute burden of hypertension (total number of individuals with
hypertension) increased by 440 million in LMICs and only 27 million in HICs.3 In 2010, the
highest absolute burden of hypertension was in East Asia and the Pacific, which had more
individuals with hypertension than all HICs combined.3 The absolute burden of hypertension
in men and women increased in all world regions between 2000 and 2010, except for in the
Middle East and North Africa where the absolute burden in women decreased slightly.3 The
Global Burden of Disease study estimated that in 2015 around 3.5 billion adults worldwide
had systolic BP of at least 110–115 mmHg, a level that is associated with increased risk of
ischaemic heart disease (IHD), stroke, and kidney disease.4 This prevalence represents a
Author Manuscript
marked increase from 1990 when 1.87 billion people had a systolic BP of at least 110–115
mmHg.4
In 2017, the American College of Cardiology/American Heart Association Task Force on

Clinical Practice Guidelines redefined hypertension in adults as systolic BP ≥130 mmHg
and/or diastolic BP ≥80 mmHg.14 This change was based on findings from a number of
large-scale, prospective observational studies that reported significant increases in risk of
CVD with increasing BP even from levels as low as systolic BP 115 mmHg, as well as the
results of randomized clinical trials including the SPRINT trial (discussed further below)
that showed that intensive BP lowering (target systolic BP <120 mmHg) reduces CVD and
all-cause mortality to an even greater extent than does standard BP lowering (target systolic
BP ≤140 mmHg).15–18 When the new definition was applied to the US general population,
Author Manuscript
hypertension prevalence increased from 32.0% (based on the traditional criteria) to 45.4%
(Table 2).19,20 In the Chinese general population, the increase was even greater from 23.2%
to 46.4%.19,20 These findings suggest that if the new criteria were applied worldwide, the
difference in hypertension prevalence between LMICs and HICs would be much greater
than previously reported.3 Full implementation of the new guidelines would require a greater
proportion of adults to be treated with antihypertensive medications but could prevent an
estimated 610,000 CVD events and 334,000 deaths per year in the US alone.19
Valid estimation of global BP levels and hypertension prevalence is highly dependent on the
availability and quality of BP data from population-based studies around the world. Many
factors, such as the representativeness of study populations (e.g. sampling methods and
response rates), BP measurement methods (e.g. calibration of BP measuring devices,
Author Manuscript
appropriate BP cuff sizes, and preparation of participants), and number of BP measurements

can affect the quality of prevalence data.21 In many countries, population-based BP studies
have not been conducted or BP data are not publicly available. In addition, the number of
studies and the quality of the available data varies substantially between regions. As a
result, BP estimates for some countries are based entirely on modelling in several pooling
projects. 4,12,22 This problem is particularly apparent in Sub-Saharan Africa for which BP
data are sparse.23 High-quality, population-based studies that accurately measure BP in all
countries

Mills et al. Page 5
worldwide, particularly in LMICs, are required to enable accurate assessment of the global
burden of hypertension.
Author Manuscript
BLOOD PRESSURE, CVD, CKD AND MORTALITY

Elevated BP is associated with a large global burden of CVD and premature death. In 2015,
the estimated number of all-cause deaths that were associated with systolic BP ≥110–115
mmHg was 10.7 million (19.2% of all deaths) and with systolic BP ≥140 mm Hg was 7.8
million (14.0% of all deaths).12 The largest numbers of deaths that were related to systolic
BP ≥110–115 mmHg were attributed to IHD (4.9 million or 54.5% of IHD deaths),
ischaemic stroke (1.5 million or 50.0% of ischaemic stroke deaths), and haemorrhagic
stroke (2.0 million or 58.3% of haemorrhagic stroke deaths) (Figure 3). The corresponding
numbers of deaths related to systolic BP ≥140 mmHg were 3.6 million (40.1% of IHD
deaths), 1.1 million (38.1% of ischemic stroke deaths) and 1.4 million (42.5% of
Author Manuscript
hemorrhagic stroke deaths).12 Consistent with trends in hypertension prevalence, the

estimated numbers of BP-related all-cause and CVD deaths increased substantially from
1990 to 2015, especially in LMICs.12 Scaling up effective antihypertensive interventions to
reduce BP-related morbidity and mortality should be a global public health priority.
Observational epidemiological studies have shown a strong, independent and linear

association between BP and the risk of CVD without any evidence of a BP threshold. 15,24–26
For example, the Prospective Studies Collaboration examined the association between BP
and cause-specific mortality in approximately 1 million adults aged 40–89 years with no
previous history of CVD at baseline using data from 61 prospective observational studies.15
During 12.7 million person-years of follow-up, around 56,000 CVD deaths (12,000 stroke,
34,000 IHD, and 10,000 other CVD) and 66,000 deaths owing to other causes were
reported. Meta-analyses that corrected for regression dilution showed that the proportional
Author Manuscript
difference in risk of CVD death that was associated with a given absolute difference in usual
BP for each decade of age was similar for increases in BP from levels as low as 115 mmHg
systolic and 75 mmHg diastolic.15 In those aged 40–69 years, a difference in usual systolic
BP of 20 mmHg or usual diastolic BP of 10 mmHg was associated with a more than twofold
difference in the rate of stroke deaths and a twofold difference in the rate of death owing to
IHD and other CVD causes. The proportional difference in CVD mortality that was
associated with a given absolute difference in usual blood pressure in adults aged 80–89
years was about half that of adults aged 40–49 years, but the annual absolute differences in
risk were greater in old age.15
In adults who are middle aged or older (≥35 years), systolic BP is a more important
determinant of CVD risk than diastolic BP.24–26 Among 347,978 men aged 35 to 57 years
Author Manuscript
who were screened in the US for entry into the Multiple Risk Factor Intervention Trial
(MRFIT) and had not previously been hospitalized for CVD, 7,150 deaths from IHD and
733 deaths from stroke were identified during an average of 11.6 years of follow-up.25 In
every decile of BP, systolic BP was more strongly associated with risk of IHD and stroke
than was diastolic BP. When the highest deciles were compared with the lowest deciles,
the relative risks associated with increased systolic and diastolic BP were 3.7 and 2.8,
respectively, for IHD, and 8.2 and 4.4, respectively, for stroke.

Mills et al. Page 6
Several large prospective cohort studies have reported that elevated BP is also a strong
independent risk factor for chronic kidney disease (CKD) and end-stage renal disease
Author Manuscript
(ESRD).27–29 The increase in risk that was associated with higher BP was dose-response and
continuous throughout the distribution of BP levels above 120 mmHg.27–29 Among 332,544
men aged 35 to 57 years who were screened for entry into the MRFIT trial and did not have
ESRD at baseline, a strong independent linear relationship between both systolic and
diastolic BP and incidence of ESRD was identified during an average of 16 years of follow-
up.28 Compared with normotensive men who had a systolic BP <120 mmHg and diastolic
BP <80 mmHg, the relative risk of ESRD for men with hypertension who had a systolic BP
>210 mmHg or diastolic BP >120 mmHg was 22.1 (P<0.001). A similar association
between BP and risk of ESRD was reported in a cohort of 158,365 Chinese men and
women aged ≥40 years.29 In addition, BP was significantly and independently associated
with progression to ESRD among patients with CKD.27 Among 3,708 patients with CKD in
the Chronic Renal Insufficiency Cohort Study in the US, multivariable-adjusted relative risk
Author Manuscript
(95% CI) for ESRD was 2.37 (CI, 1.48 to 3.80) and 3.37 (CI, 2.26 to 5.03) among those
with systolic BP of 130–139 and ≥140 mmHg, respectively, compared with systolic BP
<120 mmHg.27
Randomized clinical trials have demonstrated that BP lowering with commonly used
regimens, such as diuretics, angiotensin-converting-enzyme inhibitors, angiotensin-receptor
blockers, and calcium channel blockers reduces the risk of CVD and all-cause mortality.30,31
A large meta-analysis of 123 clinical trials with 613,815 participants showed that relative
risk reductions of CVD and all-cause mortality were proportional to the magnitude of
achieved BP reductions.31 For example, every 10 mmHg reduction in systolic BP
significantly reduced the risk of major CVD events by 20% (relative risk 0.80, 95% CI
0.77– 0.83), IHD by 17% (relative risk 0.83, 0.78–0.88), stroke by 27% (relative risk 0.73,
Author Manuscript
0.68–
0.77), heart failure by 28% (relative risk 0.72, 0.67–0.78), and all-cause mortality by 13%
(0.87, 0.84–0.91).31 This study provided no clear evidence that proportional risk reductions
in major CVD events differed by baseline BP levels or comorbidities, except for patients
with diabetes and CKD, for whom the risk reductions were smaller but still statistically
significant.
The Systolic Blood Pressure Intervention Trial (SPRINT) randomly assigned 9,361 patients
with systolic BP ≥130 mmHg and increased CVD risk to a systolic BP target of <120
mmHg (intensive treatment) or <140 mmHg (standard treatment).17 Increased CVD risk was
defined as clinical or subclinical CVD, CKD, a 10-year risk of CVD of ≥15% according to
the Framingham risk score, or an age of ≥75 years. At 1 year, mean systolic BP was 121.4
Author Manuscript
mmHg in the intensive treatment group and 136.2 mmHg in the standard-treatment group.
Moreover, intensive treatment was associated with a 25% reduction in CVD events
(hazard ratio 0.75, 95% CI 0.64–0.89, P<0.001) and a 27% reduction in all-cause mortality
(hazard ratio 0.73, 95% CI 0.60–0.90, P=0.003) compared to standard treatment over a
median follow-up of 3.26 years. The number needed to treat (NNT) to prevent one CVD
event during the follow-up period was 61, and the NNT to prevent one death from any
cause was
90.17 The SPRINT trial demonstrates that intensive BP lowering treatment with a systolic
BP target of <120 mmHg is beneficial for patients with hypertension who are at high risk of

Mills et al. Page 7
CVD. The SPRINT trial prompted the revision of the definition of hypertension and BP
antihypertensive treatment goals.14
Author Manuscript
The results of meta-analyses of randomized controlled trials that compared the efficacy of
different BP targets or treatment intensities to reduce the risk of CVD and mortality in
patients with hypertension are consistent with the SPRINT findings.18,31,32 For example, a
2015 network meta-analysis of 42 trials that included 144,220 patients with hypertension,
reported linear associations between mean achieved systolic BP and risk of CVD and
mortality, with the lowest risk among those who achieved a systolic BP of 120–124 mmHg.
18 In these trials, study groups that achieved mean systolic BPs of 120–124 mm Hg had
hazard ratios for major CVD of 0.71 (95% CI, 0.60–0.83), 0.58 (95% CI, 0.48–0.72), 0.46
(95% CI, 0.34–0.63), and 0.36 (95% CI, 0.26–0.51), compared with study groups that
achieved systolic BPs of 130–134 mmHg, 140–144 mmHg, 150–154 mmHg and ≥160
mmHg, respectively.18 Network meta-analyses offer a unique advantage over traditional
Author Manuscript
meta-regression methods by enabling the simultaneous comparison of the effects of

multiple interventions or treatment targets on clinical outcomes while preserving trial-level
treatment randomization and its associated protection against bias.
Despite the findings from SPRINT and related meta-analyses, some concerns remain about
the appropriateness and effectiveness of intensive BP reduction in certain subgroups,
including patients with CKD, diabetes or stroke and older adults (≥65 years). A pre-
specified subgroup analysis of outcomes in SPRINT trial participants with CKD found that
intensive BP treatment resulted in significant reductions in the risk of CVD and death but no
significant increase in the incidence of serious adverse events compared to standard BP
treatment.33 The rate of continuous eGFR decline was higher in the intensive BP treatment
group but there was no significant difference in risk of CKD progression (defined as
Author Manuscript
incident ESRD or halving of eGFR) between the two groups.33 In addition, a subgroup
analysis of 978 SPRINT participants (519 in the intensive and 459 in the standard treatment
group) showed that while eGFR was lower in the intensive treatment compared to standard
treatment group, urine biomarkers of tubule function, injury, inflammation, and repair were
not different over 4 years of follow-up. These findings suggest that observed eGFR declines
in the intensive treatment group predominantly reflect hemodynamic changes rather than
intrinsic damage to kidney tubule cells.34 An additional SPRINT subgroup analysis in
patients aged ≥75 years reported that intensive BP treatment significantly reduced the
incidence of CVD and mortality with no increase in serious adverse events compared with
standard BP-lowering treatment.35
As patients with diabetes or stroke were not included in the SPRINT trial, questions
regarding the risks and benefits of intensive BP lowering remain in these subgroups. The
Author Manuscript
Action to Control Cardiovascular Risk in Diabetes (ACCORD) study reported that intensive
BP treatment aimed at achieving a systolic BP target of <120 mmHg did not significantly
reduce the risk of CVD events compared with standard BP treatment (systolic BP target of
<140 mmHg) in patients with type 2 diabetes (hazard ratio 0.88; 95% CI 0.73–1.06).36
However, a subgroup analysis suggested a significant reduction in CVD events in the
intensive BP treatment group compared to standard treatment group (hazard ratio 0.74, 95%
CI 0.55 to 1.00, p=0.049) among participants who received standard glycaemic treatment.37

Mills et al. Page 8
In addition, a meta-analysis of four randomized clinical trials with 4,895 participants

reported that intensive BP control reduced the risk of recurrent stroke compared with
Author Manuscript
standard BP control (relative risk 0.78; 95% CI 0.64–0.96; P = 0.02).38 On-going clinical
trials (such as the OPTIMAL-DIABETES trial [NCT04040634], the OPTIMAL Stroke trial
[NCT04036409], the BPROAD trial [NCT03808311], and the IBIS Trial [NCT03585595])
will likely provide definite answers regarding optimum BP treatment goals for patients
with diabetes or stroke. However, the currently available evidence supports a more
intensive BP treatment target.14
RISK FACTORS FOR HYPERTENSION

BP levels and hypertension prevalence increase with age in both sexes.39 Men have higher
BP at younger ages than women, but BP increase per decade is higher in women than in
men. By the age of 60 years, women have a higher mean BP and hypertension prevalence
Author Manuscript
than men. Race and ethnicity is also a significant risk factor for hypertension. For example,
a study that analyzed National Health and Nutrition Examination Survey (NHANES) 2015–
2016 data for 4,821 US adults aged ≥20 years, reported a significantly higher age-
standardized prevalence of hypertension in non-Hispanic Black individuals (57.3%) than in
non-Hispanic White individuals (43.8%) and Hispanic-Americans (44.7%).40 There is no
evidence that racial and ethnic disparities in risk of hypertension are explained by genetic
factors.41,42 Sociodemographic, environmental and behavioral factors are therefore likely to
be the main contributors to racial and ethnic differences in mean BP and prevalence of
hypertension.42 In addition, several modifiable risk factors, including high sodium intake,
low potassium intake, alcohol consumption, obesity, lack of physical activity, and unhealthy
diet are associated with increased risk of hypertension
Author Manuscript
High sodium intake

The PURE study estimated that in 2010, global sodium intake was 3,950 mg per day, which
is considerably higher than the recommended amounts of 2,300 mg or less per day in all
published guidelines.44,45 In addition, sodium consumption varied considerably by world
region from >4,200 mg per day in East Asia, Central Asia, and Eastern Europe to <3,300 mg
per day in Latin America and Sub-Saharan Africa.44
Animal experiments, observational epidemiologic studies, and randomized clinical trials

have demonstrated a causal relationship between sodium intake and elevated BP.46 The
majority of the observational studies were cross-sectional and reported a positive, linear,
and significant association of either dietary intake or 24-hour urinary excretion of sodium
with BP or hypertension.47,48 For example, the Intersalt study investigated the association
Author Manuscript
between 24-hour urinary sodium excretion and BP among 10,074 men and women aged 20–
59 from 52 population samples in 32 countries.47 In within population analyses, a 100 mmol
higher individual 24-hour urinary sodium excretion was associated with a 6.0 mmHg higher
average systolic BP and a 2.5 mmHg higher average diastolic BP. In across population
analyses, a 100 mmol higher median 24-hour sodium excretion was associated with a
median 4.5 mmHg higher systolic and 2.3 mmHg higher diastolic BP.47 When four remote
populations with extremely low urinary sodium excretion were excluded from the across

Mills et al. Page 9
population analyses, a 100 mmol increase in median 24-hour sodium excretion was
associated with a 2.5 mmHg increase in systolic BP.47 The Intersalt study showed consistent
Author Manuscript
patterns of regional differences in salt intake and BP levels. A positive and significant
association between spot urinary sodium excretion and BP was also observed in the PURE
study.49
In the DASH-Sodium trial, 412 people with an average systolic BP of 120–159 mmHg and
diastolic BP of 80–95 mmHg were randomly assigned to high sodium (mean urinary
excretion of 142 mmol per day), intermediate sodium (mean urinary excretion of 107 mmol
per day) and lower sodium diets (mean urinary excretion of 65 mmol per day) for 30 days
in a cross-over design.50 The results showed that reducing sodium intake from a high to an
intermediate level lowered systolic BP by 2.1 mmHg (P<.001) during consumption of a
usual American control diet and by 1.3 mm Hg (P = 0.03) during consumption of a Dietary
Approaches to Stop Hypertension (DASH) diet. Further reducing sodium intake from an
Author Manuscript
intermediate to a lower level resulted in an additional reduction in systolic BP of 4.6 mmHg

during consumption of the control diet (P<0.001) and a 1.7 mmHg reduction during
consumption of the DASH diet (P<0.01).50
Several meta-analyses of clinical trials have shown that sodium reduction significantly
lowers BP in hypertensive and normotensive individuals.51–55 An Agency for Healthcare
Research and Quality (AHRQ) meta-analysis that included 48 randomized control trials
found a significant BP-lowering effect of dietary sodium reduction in adults both with and
without hypertension.55 In this study, a 42 mmol decrease in the weighted mean sodium
intake was associated with a 3.23 mmHg (95% CI 2.41–4.06) reduction in systolic BP and a
2.24 mmHg (95% CI 1.61–2.96) reduction in diastolic BP.55
Despite the strong positive association between dietary sodium intake, BP and risk of
Author Manuscript
hypertension, the associations of sodium intake with risk of CVD, CKD, and mortality are
inconsistent.55 Some studies have found a positive association between dietary sodium
intake and these clinical outcomes, whereas others have found inverse, J-shaped or U-
shaped associations.56–65 These conflicting findings can likely be partly explained by
methodological limitations, such as systematic and random error in sodium measurements,
reverse causality, insufficient statistical power, residual confounding, and inadequate
follow- up duration.55,64,66 In summary, dietary sodium reduction should be recommended
to lower population BP levels and risk of hypertension. More research is needed, however,
to determine optimal dietary sodium intake for the prevention of CVD, CKD and mortality.
Low potassium intake

Similar to sodium, considerable regional variation exists in 24-hour urinary potassium
Author Manuscript
excretion (the best available measure of potassium intake) with the highest levels in Europe
(e.g., Finland 2,995 mg, Netherlands 2,835 mg, Germany 2,825 mg, Belgium 2,618 mg, and
Spain 2,629 mg) and South America (e.g., Brazil 2,940 mg, and Colombia 2,803 mg), and
the lowest levels in Asia (e.g., China 1,249 mg and Japan 1,792 mg) and Africa (e.g., Kenya
1,306 mg and Zimbabwe 1,466 mg).67,68 Observational epidemiological studies have
reported an inverse association of dietary potassium intake with BP levels and hypertension.
In the Intersalt study, a 50 mmol per day higher level of urinary potassium excretion was

Mills et al. Page 10
associated with a 3.4 mmHg (95% CI 1.5–5.2) lower level of systolic BP and 1.9 mmHg
(95% CI 0.7–3.0) lower level of diastolic BP after adjustment for important confounding
Author Manuscript
factors, including age, sex, BMI, alcohol consumption, and urinary sodium excretion, and
correction for regression dilution bias.69
Randomized clinical trials have shown that potassium supplementation lowers BP in

hypertensive and normotensive individuals.70–73 In a meta-analysis of 33 randomized
controlled trials with 2,609 participants, potassium supplementation was associated with
significant reductions in mean systolic and diastolic BP of 3.11 mmHg (95% CI 1.91–4.31)
and 1.97 mmHg (95% CI 0.52–3.42), respectively.71 In 31 trials with urinary potassium
measurements, the median net increase in potassium excretion in the potassium
supplementation group versus the control group was 50 mmol per day; in 21 (68%) of these
trials, the net difference in potassium excretion was ≥40 mmol per day. 71 The effects of
potassium supplementation seemed to be greater in black individuals and in those eating a
Author Manuscript
high sodium diet. An AHRQ meta-analysis that included 18 randomized controlled trials
also reported that potassium supplementation was associated with a significant reduction in
systolic (6.43 mmHg; 95% CI 1.80–11.1) and diastolic BP (3.50 mmHg; 95% CI 0.89–
6.10).55 Increasing potassium intake, especially from fruits and vegetables, is therefore
recommended for the prevention and treatment of hypertension.14,43
Alcohol consumption—Globally, alcohol consumption varies considerably, with the

lowest consumption in North African and the Middle East (most countries <1 L per-capita
annually), and the highest consumption in Central and Eastern Europe (many countries >12
L per-capita annually). Global annual alcohol consumption increased from 5.9 L per-capita
in 1990 to 6.5 L in 2017.74 Numerous observational epidemiologic studies have reported
that high alcohol consumption is a risk factor for elevated BP.75,76 The Atherosclerosis
Author Manuscript
Risk in Communities Study reported a J-shaped association between alcohol consumption

and risk of hypertension.76 Light to moderate alcohol drinkers were at lower risk of incident
hypertension than nondrinkers, whereas heavy drinkers were at higher risk than both light
to moderate drinkers and nondrinkers. This pattern was observed in all race and gender
groups except for black men, for whom risk was similarly elevated in light to moderate and
heavy drinkers compared to nondrinkers.76 In a large prospective cohort study of over
500,000 Chinese adults, however, self-reported usual alcohol intake and genotype-predicted
alcohol intake were both positively and linearly associated with BP. Genetic
epidemiological data showed that the observed protective effects of moderate alcohol intake
against hypertension and CVD were largely non-causal.77
A meta-analysis of 15 randomized control trials with a total of 2,234 participants reported

Author Manuscript
that a reduction in alcohol intake (median: 76%, range: 16%–100%) was associated with
significant reductions in mean systolic BP (3.31 mmHg, 95% CI 2.52–4.10) and diastolic BP
(2.04 mmHg, 95% CI 1.49–2.58).78 A dose-response relationship was observed between
mean percentage reduction in alcohol intake and mean reduction in BP. Moreover, the
effects of reducing alcohol intake on BP were enhanced in those with higher BP at baseline.
A recent meta-analysis of 36 trials with 2,865 participants showed that a reduction in alcohol
intake was not associated with a significant reduction in BP in individuals who drank two or
fewer drinks per day. However, a 50% reduction in alcohol intake was significantly

associated with a 5.50 (95% CI 4.30 to 6.70) mmHg lower systolic BP and a 3.97 (3.25 to
4·70) mmHg lower diastolic BP in participants who drank six or more drinks per day.79
Author Manuscript
These findings suggest that reducing alcohol intake should be recommended as an

important component of lifestyle modification for the prevention and treatment of
hypertension in people who are heavy drinkers.
Lack of physical activity

Global age-adjusted prevalence of insufficient physical activity (less than 150 min of
moderate-intensity, or 75 min of vigorous-intensity physical activity per week, or any
equivalent combination of the two) was 27.5% with a higher prevalence in women (31.7%)
than in men (23.4%). The highest levels were in women in Latin America and the
Caribbean (43.7%), south Asia (43.0%), and high-income Western countries (42.3%),
whereas the lowest levels were in men from Oceania (12.3%), east and southeast Asia
(17.6%), and sub- Saharan Africa (17.9%). Prevalence of insufficient physical activity was
Author Manuscript
much higher in urbanized populations in high-income countries.80
Epidemiological studies have reported an inverse relationship between physical activity,

BP and hypertension.81 Even modest levels of physical activity (such as walking to work)
are associated with a decrease in the risk of incident hypertension.82 Randomized
controlled trials and meta-analyses have demonstrated that physical activity lowers BP in
hypertensive and normotensive individuals.83–85 For example, a meta-analysis of 54
randomized controlled trials with 2,419 participants reported that aerobic exercise was
associated with a significant reduction in mean systolic BP of 3.84 mmHg (95% CI 2.72–
4.97) and diastolic BP of 2.58 mmHg (95% CI 1.81–3.35).83 Aerobic exercise-induced BP
reductions were consistent in hypertensive and normotensive participants and in
overweight and normal- weight participants. These findings indicate that physical activity
Author Manuscript
is an effective lifestyle intervention for the prevention and treatment of hypertension.
Overweight and obesity

The prevalence of obesity has increased rapidly worldwide over the past several decades.
From 1975 to 2014, global age-standardized prevalence of obesity increased from 3.2% to
10.8% in men, and from 6.4% to 14.9% in women. During the same period, global age-
standardized mean body mass index (BMI) increased from 21.7 kg/m2 to 24.2 kg/m2 in men
and from 22.1 kg/m2 in 1975 to 24.4 kg/m2 in women. BMI varied significantly by world
region, from 21.4 kg/m2 in central Africa and south Asia to 29.2 kg/m2 in the Pacific Islands
for men and from 21.8 kg/m2 in south Asia to 32.2 kg/m2 in the Pacific Islands for women in
2014.86
Author Manuscript
Epidemiological studies have consistently identified a direct relationship between BMI and
BP that is continuous and almost linear, with no evidence of a threshold.87,88 The
relationship between BP and waist-to-hip ratio or computed tomographic measures of
central fat distribution is even stronger than the relationship between BP and BMI.89
Attributable risk estimates from the Nurses’ Health Study suggest that obesity is
responsible for about 40% of hypertension80, whereas the Framingham Offspring Study
suggested that obesity is responsible for 78% of hypertension in men and 65% of
hypertension in women.

90,91In a meta-analysis of 25 randomized controlled trials with 4,874 participants, a net

reduction in body weight of 5.1 kg (95% CI 4.25–6.03) owing to calorie restriction,
Author Manuscript
increased physical activity, or both, reduced systolic BP by 4.44 mmHg (95% CI 2.95–
5.93) and diastolic BP by 3.57 mmHg (95% CI 2.25–4.88). BP reductions were 1.05 mmHg
(95%
CI 0.66–1.43) systolic and 0.92 mmHg (95% CI 0.55–1.28) diastolic when expressed per
kilogram of weight loss.92
Unhealthy diet
In addition to sodium and potassium, several macronutrients are associated with BP,
including dietary fiber,93,94 protein,95,96 and fat.97,98 The Global Burden of Diseases
Nutrition and Chronic Diseases Expert Group examined two different dietary patterns
worldwide: one based on relatively high consumption of ten healthy items (fruits,
Author Manuscript
vegetables, beans and legumes, nuts and seeds, whole grains, milk, total polyunsaturated
fatty acids, fish, plant omega-3s, and dietary fiber); and another based on relatively low
consumption of seven unhealthy items (unprocessed red meats, processed meats, sugar
sweetened beverages, saturated fat, trans fat, dietary cholesterol, and sodium). Diets and
their trends were very heterogeneous across world regions. For example, both types of
dietary patterns improved in high-income countries but worsened in some low-income
countries in Africa and Asia. Middle-income countries showed the largest improvement in
dietary patterns based on healthy items but the largest deterioration in dietary patterns based
on unhealthy items.99
The efficacy of dietary interventions for blood pressure lowering has been investigated in
randomized controlled trials. For example, in the DASH trial, 459 adults with systolic BP
<160 mmHg and diastolic BP of 80–95 mm Hg were randomly assigned to 8 weeks of a
Author Manuscript
control diet low in fruits, vegetables, and dairy products with a fat content typical of the
average diet in the US, a diet rich in fruits and vegetables or a DASH diet rich in fruit,
vegetables and low-fat dairy products with a total fat and saturated fat content lower than
the
typical US diet.100 Sodium intake and body weight were maintained at constant levels.
Compared to the control diet, the DASH diet significantly reduced systolic and diastolic BP
by 5.5 mmHg and 3.0 mmHg (both P<0.001), respectively, whereas the fruit and vegetable
diet reduced systolic and diastolic BP by 2.8 mmHg (P<0.001) and 1.1 mm Hg (P=0.07),
respectively. In participants with hypertension, the DASH diet reduced systolic and
diastolic BP by 11.4 mmHg and 5.5 mmHg compared with the control diet (both P<0.001).
The DASH diet was also effective in reducing BP in normotensive participants, but the BP
reductions were smaller than those seen in hypertensive participants [(3.5 mmHg (P<0.001)
Author Manuscript
and 2.1 mmHg (P=0.003) compared with the control diet].100 These data indicate that the
DASH diet provides an effective nutritional approach to prevent and treat hypertension.
Vegetarian and Mediterranean dietary patterns are also associated with BP reduction. 101,102
A meta-analysis of 7 randomized controlled trials with a total of 311 participants reported
that vegetarian diets (defined as diets that never or rarely included meat) were associated
with a mean reduction in systolic BP of 4.8 mmHg (95% CI 3.1–6.6) and diastolic BP of 2.2
mmHg (95% CI 1.1–3.5).101 Mediterranean diets are characterized by moderate fat intake
(primarily from olive oil and nuts), low consumption of red meat, and high consumption of
vegetables.102 A meta-analysis of 6 trials with a total of 2,650 participants reported a modest

but significant reduction in systolic BP of 1.7 mmHg (95% CI 0.1–3.4) and diastolic BP of
Author Manuscript
1.5 mmHg (95% CI 0.8–2.1) in Mediterranean diets compared to low-fat diets.102
In summary, numerous lifestyle risk factors are associated with BP levels and
hypertension. These risk factors vary by world region and this heterogeneity likely
underlies some of the disparities in hypertension trends and prevalence worldwide.
Lifestyle interventions that target these risk factors could therefore play an important role
in reducing global disparities in hypertension.22 Implementing lifestyle interventions in
HICs has contributed to reductions in hypertension prevalence and BP levels.43 However,
there is limited data on implementing lifestyle intervention programs in LMIC
communities.
Other potential risk factors

Author Manuscript
Several other potential risk factors for hypertension have been proposed, including cigarette
smoking, air pollution, psychological stress, sleep disorders and noise exposure. 103–114
Cigarette smoking has been shown to be associated with an immediate acute increase in
BP, mainly through stimulation of the sympathetic nervous system.103,104,107 However, its
long- term effects on BP and incidence of hypertension are inconclusive.107,108,115 Several
prospective cohort studies have reported a weak positive association between cigarette
smoking and risk of hypertension. For example, in 13,529 men from the Physicians’ Health
Study, former and current smoking were significantly associated with an 8% (RR 1.08,
95% CI 1.01 to 1.15) and 15% (RR 1.15, 95% CI 1.03 to 1.27) increase in the risk of
incident hypertension, respectively, compared with never smoking over a median follow-up
of 14.5 years.107 In a prospective cohort study of 28,236 women from the Women’s Health
Study, multiple-adjusted hazard ratios of developing hypertension among former smokers
Author Manuscript
and current smokers of 1–14 and ≥15 cigarettes per day were 1.03 (95% CI 0.98 to 1.08),
1.02
(95% CI 0.92 to 1.13), and 1.11 (95% CI 1.03 to 1.21), respectively, compared to never
smokers.108 However, direct causality between cigarette smoking and hypertension
cannot be established because cessation of chronic smoking does not lower BP.116
The association between exposure to ambient air pollutants and risk of hypertension has
been investigated in epidemiological studies.109,110 A meta-analysis that examined the
effects of a 10 µg/m3 increase in exposure to air pollutants on hypertension, reported that
short-term exposure over several days to sulfur dioxide (OR=1.046, 95% CI 1.012–1.081),
particulate matter with a diameter of ≤2.5 µm (PM2.5) (OR=1.069, 95% CI 1.003–1.141),
and particulate matter with a diameter of ≤10 µm (PM10) (OR=1.024, 95% CI 1.016–1.032)
Author Manuscript
were all significantly associated with hypertension (based on data from 7 studies). 109 Long-
term exposure over years to nitrogen oxide (OR=1.034, 95% CI 1.005–1.063) and PM10
(OR=1.054, 95% CI 1.036–1.072) were also significantly associated with hypertension
(based on data from 11 studies). These results suggest that short-term and long-term
exposure to air pollutants might increase the risk of hypertension. Future studies are needed
to assess the impacts of chronic exposure to air pollution on global disparities of
hypertension.117,118
Psychosocial stress and rotating shift work have also been reported to be associated with
risk of hypertension.111,112 In a meta-analysis of two observational studies with 622
participants,

mental stress was associated with an increased risk of hypertension (OR 2.40, 95% CI 1.65–
3.49, p < 0.001).111 However, a meta-analyses of 15 trials with 902 participants testing the
Author Manuscript
effects of different stress-reduction techniques, such as biofeedback, relaxation or combined

interventions, on BP concluded that the benefit of stress reduction on BP remains unproven.
119 The meta-analysis identified methodological shortcomings in these trials and significant
heterogeneity of BP changes: from −12 to 10 mmHg for systolic and from −10 to 1 mmHg
for diastolic. In addition, a meta-analysis of 9 cohort studies with a total of 172,824
individuals reported a pooled OR of hypertension in shift workers of 1.31 (95% CI, 1.07–
1.60).112 In addition, ambient noise from road, rail, and air traffic has a modest association
with hypertension prevalence but not incidence in cohort studies.113,114 An inconsistent
relationship between sleep duration and risk of hypertension has also been reported. 105
Obstructive sleep apnea is a very common risk factor for hypertension, and continuous
positive airway pressure was shown to reduce systolic BP by 2.46 mm Hg (95% CI 0.62–
Author Manuscript
4.31) and diastolic BP by 1.83 mm Hg (95% CI 0.61–3.05) in a meta-analysis of 16

randomized clinical trials with 818 participants.106
In summary, observational studies have reported weak or moderate associations between

these potential risk factors (i.e., cigarette smoking, air pollution, psychological stress, sleep
disorders and noise exposure) and risk of hypertension. However, there is insufficient
evidence from randomized clinical trials to support causal relationships between these
potential risk factors and risk of hypertension. Overall, the currently available data suggest
that these potential risk factors have limited effect on BP in the general population.
HYPERTENSION CONTROL IN THE COMMUNITY

As discussed above, antihypertensive treatment and lifestyle modifications have been
Author Manuscript
shown to lower BP and CVD risk in randomized clinical trials.30,31,120,121 Despite these
effective interventions, hypertension control remains unacceptably low, particularly in
LMICs.3 The most recent global estimates suggest that in 2010, only 45.6% of people with
hypertension were aware of their condition, only 36.9% were receiving treatment, and only
13.8% had achieved BP control (defined as systolic BP <140 mmHg and diastolic BP <90
mmHg.3 Moreover, HICs had approximately twice the proportion of hypertension
awareness and treatment and four times the proportion of hypertension control than that of
LMICs, in which the proportion of BP control was only 7.7% in 2010.3 Between 2000 and
2010, HICs experienced substantial improvements in the proportions of hypertension
awareness, treatment, and control. In the same period, awareness and treatment increased
much more modestly in LMICs and the proportion of patients with hypertension and
controlled BP decreased slightly (Table 3).3 Similar patterns were observed in the baseline
Author Manuscript
data from the PURE study in which hypertension awareness, treatment, and control were
lower in communities in low-income countries (LICs) than in those in HICs.11
Large-scale screening programs in communities or health facilities could be an effective

way to address the lack of BP awareness in LMICs. For example, May Measurement Month
(MMM) 2017 was a BP screening program aimed at raising global awareness of
hypertension.122 The MMM 2017 program screened over 1.2 million individuals in 80
countries who had not had their BP measured in the past year and found that 34.9% had

hypertension, 17.3% of those with hypertension were not receiving treatment, and 46.3% of
those with hypertension who were receiving treatment did not have controlled BP (systolic
Author Manuscript
BP ≥140 mmHg or diastolic BP ≥90 mmHg). This program demonstrated that BP screening
in convenience samples can be cost-effective and can identify large numbers of individuals
who could benefit from initiation or enhancement of antihypertensive treatment.122
Barriers to hypertension control exist at multiple levels: patients, healthcare providers,

health systems, and communities.123–125 A meta-analysis of randomized controlled trials
that assessed the comparative effectiveness of 8 implementation strategies for BP control in
patients with hypertension found that multilevel, multicomponent strategies were most
effective for systolic BP reduction.125 These multicomponent strategies included team-based
care with medication titration by a nonphysician mean change −7.1 mmHg, 95% CI −8.9 to
−5.2 mmHg]), team-based care with medication titration by a physician (−6.2 mmHg 95%
CI, −8.1 to −4.2 mmHg), and multilevel strategies without team-based care (−5.0 mmHg,
Author Manuscript
95% CI, −8.0 to −2.0 mmHg). Patient-level strategies resulted in systolic BP reductions of
−3.9 mmHg (95% CI, −5.4 to −2.3 mm Hg) for health coaching and −2.7 mmHg (95% CI,
−3.6 to −1.7 mm Hg) for home BP monitoring. Similar trends were reported for diastolic BP
reductions. Strategies that targeted provider-level barriers only, including provider training,
audit and feedback, and electronic decision support systems, did not result in significant BP
reductions.
Most trials of implementation strategies to overcome barriers to BP control have been

conducted in HICs. Whether the same strategies will be effective in LMICs is unclear. A
cluster-randomized trial published in 2017 showed that a multifaceted intervention, which
included a community health worker-led home intervention (health coaching, home BP
monitoring, and BP audit and feedback), a physician intervention, and a text-messaging
Author Manuscript
intervention over 18 months, significantly lowered systolic BP by 6.6 mmHg (95% CI, 4.6–
8.6; P <0.001) and diastolic BP by 5.4 mmHg (95% CI, 4.0–6.8 mmHg; P <0.001) in low-
income patients in Argentina.126 This trial indicated that a community health worker-led
multifaceted intervention was effective for improving patients’ adherence to
antihypertensive medication and physicians’ adherence to clinical guidelines resulting in a
significant reduction in BP and an increase in hypertension control among low-income
patients with hypertension. Widespread scale-up of this proven effective intervention in
LMICs should result in a substantial reduction in uncontrolled hypertension and related
CVD and premature death.
Increased use of out-of-office BP measurements for confirmation of hypertension diagnosis

and titration of antihypertensive medications could also play an important role in improving
BP control. A meta-analysis of 11 prospective cohort studies showed that ambulatory BP
Author Manuscript
measurements (ABPM) predicted long-term CVD outcomes independently of office BP

(hazard ratio range, 1.28 to 1.40).127 An international pooling project with 11,135
participants reported that higher 24-hour and night-time BP measurements using ABPM
were significantly associated with greater risks of death and CVD outcomes after
adjustment for office BP.128 However, the incremental improvement in predictive values of
clinical outcomes with these measurements compared with office BP was small. Adding 24-
hour or nighttime systolic BP to base models that included other BP measures resulted in

incremental improvements in the area under the curve (AUC) of 0.0013 to 0.0027 for
mortality and 0.0031 to 0.0075 for CVD.128 However, base models that included single
Author Manuscript
systolic BP measure already had an AUC of 0.83 for mortality and 0.84 for CVD. Home
BP measurements (HBPM) are a more economical option than ABPM and are a useful
strategy to overcome patient-level barriers to BP control by empowering patients.129 Use of
self HBPM resulted in a significant reduction in systolic and diastolic BP among patients
with hypertension in randomized clinical trials.125,130 Out-of-office BP measurements are
recommended for diagnostic confirmation to avoid white coat hypertension and masked
hypertension and for optimal titration of medications to overcome therapeutic inertia.130
The prevention and control of hypertension in communities requires a life-course approach.

131 Epidemiological studies have shown that elevated BP in childhood promotes subclinical
organ damage (i.e. early vascular ageing) and leads to increased risk of hypertension, CVD,
and CKD later in life.132–134 To reduce BP-related risks of CVD, CKD, and premature
Author Manuscript
death over the lifespan, preventive efforts should start in early childhood. Innovative
strategies for early detection and optimal treatment of hypertension, such as a multifaceted
intervention approach, should be implemented in communities to reduce the burden of this
condition.
THE FINANCIAL BURDEN OF HYPERTENSION

Hypertension is associated with a substantial financial burden. Costs include direct
healthcare expenditures associated with BP management, such as medications, laboratory
tests, and clinic visits, as well as costs associated with hospitalizations for BP-related
complications and indirect costs associated with lost productivity resulting from premature
mortality and disability owing to hypertension-related cardiovascular and kidney diseases.
Author Manuscript
135 The global financial burden of high BP in 2001 was estimated to be around 370 billion
US dollars or about 10% of the world’s overall healthcare expenditure.135 However, large
regional variations in healthcare costs were observed. For example, high BP accounted for
22.6% of all healthcare expenditures in Eastern Europe and Central Asia but only 7.2% in
East Asia and Pacific.135 To the best of our knowledge, no more recent estimates of the
global financial burden of hypertension are available.
More recent national and regional estimates of the financial burden of hypertension are
available for some HICs, although they are not always consistent owing to methodologic
differences.136–139 A study that used a nationally representative database, the Medical
Expenditure Panel Survey, estimated that the average annual adjusted incremental
expenditure for patients with hypertension was $1,920 higher compared to individuals
Author Manuscript
without hypertension in the US between 2003 and 2014. Based on an average annual
number of individuals with hypertension in the US (n= 68,420,747) from NHANES during
this period, the estimated adjusted annual incremental cost is $131 billion higher for the
hypertensive adult population compared with the non-hypertensive population..136 Using
the same database, another study analyzed changes in medical expenditures associated with
hypertension between 2000 and 2013. Estimated annual medical expenditures per person
associated with hypertension in 2000–2001 ($1,399) were not significantly different from
those in 2012–2013 ($1,494), but annual national spending for patients with hypertension
increased significantly from US$58.7 billion in 2000–2001 to US$109.1 billion in 2012–

2013, mainly owing to an increase in the number of treated patients.137 In addition to lower
estimates of medical costs per patient, the underestimated prevalence of hypertension in the
Author Manuscript
Medical Expenditure Panel Survey which used self-reported history of hypertension to

define hypertension might also contribute to the conservative estimates of medical
expenditure for hypertension in this study.121
Payments for prescription medications account for a large proportion of the medical
expenditures associated with hypertension. The cost of hypertension medication
expenditures in the US in 2007 was estimated to be $68 billion based on an analysis of data
for 21,782 adults (aged ≥18 years) who participated in the Medical Expenditure Panel
Survey.139 A study that used data from the National Hospital Discharge Survey reported
that annual costs for hypertension-related hospitalizations in the US increased from $40
billion (5.1% of total hospital costs) during 1979–1982 to $113 billion (15.1% of total
hospital costs) during 2003–2006.138 The American Heart Association projected that by
Author Manuscript
2030, the direct costs of hypertension in the US population would increase to $200 billion
and the indirect costs to $40 billion.140
In a study of 314, 622 beneficiaries of the medical insurance system in Japan, inpatient
medical expenditure attributable to hypertension represented 7.2% and 6.9% of the total
medical expenditure for men and 2.8% and 3.8% of the total medical expenditure for
women aged 40–54 years and 55–69 years, respectively.141 Estimates from Mexico suggest
that combined direct and indirect costs attributable to hypertension amounted to nearly $2.5
billion in 2007, which was between 6% and 8% of the healthcare budget.122 The economic
burden of hypertension in Mexico grew by 24% between 2010 and 2012, and the total direct
and indirect costs of hypertension in 2011 were estimated to exceed $5.7 billion.123
Author Manuscript
The financial implications of hypertension in LICs are of particular concern because of the
rapid increase in the prevalence and absolute burden of hypertension and the low current and
projected healthcare spending in these regions.4,124 In 2016, only 0.4% of global health
spending was in LICs even though these countries comprise 10% of the global population.
124 Projections suggest that by 2050, only 0.6% of health spending will occur in countries
that are currently classed as LICs although these countries will comprise 15.7% of the global
population.124 Many LICs currently rely on development assistance for health spending
from international agencies and private philanthropy, which is primarily focused on
infectious diseases and could be less sustainable for chronic disease control.124 Large-scale
studies using standardized methods are needed to improve understanding of the economic
costs of hypertension, particularly in LMICs.
In general, interventions are considered to be reasonably cost-effective if they cost less than
Author Manuscript
US$50,000–75,000 per quality-adjusted life year (QALY); however, payers routinely cover
treatments that cost >$100,000 per QALY.145 Several analyses have concluded that all
antihypertensive medications are cost effective compared with no treatment (placebo). 146 In
a meta-analysis of 14 studies, the incremental cost-effectiveness ratio (ICER) of all
antihypertensive medications adjusted to 2015 US dollars was $19,945 per QALY
gained.146 The SPRINT trial reported an ICER of $28,000 per QALY gained for the
intensive BP intervention compared to the standard intervention if the treatment effects
persisted for the

remaining lifetime of the patient.147 Antihypertensive treatment might be even more cost
effective in LMICs than in HICs. For example, treating all adults with hypertension and
Author Manuscript
prior CVD for secondary prevention was projected to be cost saving in China with an ICER
in 2015 of Int$9,000 per QALY gained in those with BP ≥160/100 mmHg and Int$13,000
per QALY gained in those with BP ≥140/90 mm Hg.148 Moreover, patient-centered values,
such as health-related quality of life, productivity, severity of disease, and equity, are
important to factor into analyses when determining the financial burden associated with
hypertension and weighing the costs of prevention and treatment versus the costs associated
with BP-related CVD.149,150
FUTURE PERSPECTIVES
Without intervention, the prevalence and absolute burden of hypertension is expected to
continue to increase, particularly in LMICs.3,4,12,13 Consequentially, BP-related
Author Manuscript
cardiovascular and kidney disease will become even greater health and financial burdens
worldwide.2 Economic development and urbanization have resulted in rapid epidemiological
and nutrition transitions, i.e., decreasing infant mortality and infectious diseases and
increasing life expectancy and chronic diseases, in many LMICs, including China and India.
151–153 The prevalence of hypertension is high and increasing in these countries, whereas the
rates of awareness, treatment and control are low.3,20 Lifestyle risk factors for hypertension,
such as obesity, high dietary sodium intake, low dietary potassium intake, alcohol
consumption, lack of physical activity and unhealthy diet have reached epidemic proportions
in LMICs.154,155 National programs for the prevention, detection, and treatment of
hypertension in LMICs are needed to slow and reverse the current trends in the hypertension
epidemic. In addition, community-based intervention programs are needed to reduce health
disparities and improve hypertension prevention and control in low-income and ethnic
Author Manuscript
minority populations in HICs.42 To accurately estimate the global burden of hypertension,

worldwide prevalence surveys using standardized methodology for sampling of participants,
BP measurement, and data quality control and analysis are needed, especially in under-
represented regions.3 Research to develop and test the effective, equitable, and sustainable
interventions for implementing evidence-based clinical guidelines and public health policies
worldwide are critically important for reducing the global burden of hypertension.3
CONCLUSIONS
Although the estimated global mean BP appears to be fairly stable, the prevalence and
absolute burden of hypertension is increasing globally, especially in LMICs. In 2010, an
estimated 1.39 billion adults worldwide had hypertension of whom 1.04 billion were in
LMICs and 349 million in HICs.3 Elevated BP is strongly, independently, and linearly
Author Manuscript
associated with the risk of CVD, CKD, and all-cause mortality. Although effective lifestyle
modifications and pharmaceutical treatments are available, proportion of hypertension
awareness, treatment, and control are low. Hypertension, therefore, remains a global public
health challenge. Few comprehensive assessments of the economic impact of hypertension
in global populations exist. It was estimated that the global financial burden of
hypertension was about 10% of the world’s overall healthcare expenditures, varying from
about 22.6% of all healthcare expenditures in Eastern Europe and Central Asia to 7.2% in
East Asia and

Pacific. Future studies are warranted to develop multifaceted implementation strategies for
hypertension prevention and control, especially in LICs and low-income populations, and
Author Manuscript
to accurately assess the financial burden of hypertension worldwide.
Acknowledgements
The authors’ work is supported by the National Institute of General Medical Sciences of the National Institutes of
Health (NIH) under Award Number P20GM109036 and by the National Heart, Lung, and Blood Institute of NIH
under Award Number R01HL133790. The content is solely the responsibility of the authors and does not
necessarily represent the official views of NIH.
Glossary of Terms
Pooling analysis
A type of meta-analysis in which investigators have access to and analyze the
original individual level data from participating study
Author Manuscript
Regression dilution (bias)

In an epidemiological study the regression slope between a response and predictor variable
is underestimated when the predictor variable is measured imprecisely
Network meta-analysis
A type of meta-analysis in which multiple treatments are being compared using both direct
comparisons of interventions within randomized controlled trials and indirect comparisons
across trials based on a common comparator
Cross-over design
A type of clinical trial in which each participant is randomized to a sequence of two or more
treatments; therefore, the participant is used as his or her own control
Author Manuscript
Dietary Approaches to Stop Hypertension (DASH) diet

A diet emphasizing fruits, vegetables, and low-fat dairy foods; including whole
grains, poultry, fish, and nuts; and limiting red meat, sweets, and sugar-containing
beverages
Weighted mean
A type of average that instead of each of the data points contributing equally to the
final average, some data points contribute more than others
Dose-response relationship
A relationship in which a change in amount, intensity, or duration of exposure is
associated with either increasing or decreasing risk of the outcome
Author Manuscript
Convenience samples
A type of non-probability sample in which the study participants are taken from a group of
people easy to contact or to reach
Quality-adjusted life year (QALY)

A measure of the burden of disease on a defined population which equals the sum of years
of life lost (YLLs) and years lived with disability (YLDs). One DALY equals one lost
Author Manuscript
year of healthy life
Incremental cost-effectiveness ratio (ICER)

A measure of the cost-effectiveness of new health care interventions defined as the ratio
of the difference in cost between two possible interventions divided by the difference in
their effect
References
1. Stanaway JD et al. Global, regional, and national comparative risk assessment of 84
behavioural, environmental and occupational, and metabolic risks or clusters of risks for 195
countries and territories, 1990–2017: A systematic analysis for the Global Burden of Disease
Stu. Lancet 392, 1923–1994 (2018). [PubMed: 30496105]
Author Manuscript
2. GBD 2017 Causes of Death Collaborators, G. A. et al. Global, regional, and national age-sex-
specific mortality for 282 causes of death in 195 countries and territories, 1980–2017: a systematic
analysis for the Global Burden of Disease Study 2017. Lancet (London, England) 392, 1736–1788
(2018).
3. Mills KT et al. Global Disparities of Hypertension Prevalence and Control: A Systematic
Analysis of Population-Based Studies From 90 Countries. Circulation 134, 441–450 (2016).
[PubMed: 27502908]
4. Zhou B et al. Worldwide trends in blood pressure from 1975 to 2015: a pooled analysis of 1479
population-based measurement studies with 19·1 million participants. Lancet 389, 37–55
(2017). [PubMed: 27863813]
5. Falaschetti E, Mindell J, Knott C & Poulter N Hypertension management in England: a serial
cross- sectional study from 1994 to 2011. Lancet (London, England) 383, 1912–9 (2014).
6. Ezzati M et al. Contributions of risk factors and medical care to cardiovascular mortality trends.
Nat. Rev. Cardiol 12, 508–530 (2015). [PubMed: 26076950]
7. Laatikainen T, Nissinen A, Kastarinen M, Jula A & Tuomilehto J Blood Pressure, Sodium Intake,
Author Manuscript
and Hypertension Control: Lessons From the North Karelia Project. Glob. Heart 11, 191–9
(2016). [PubMed: 27242086]
8. Ibrahim MM & Damasceno A Hypertension in developing countries. Lancet 380, 611–619
(2012). [PubMed: 22883510]
9. Hogerzeil HV et al. Promotion of access to essential medicines for non-communicable diseases:
practical implications of the UN political declaration. Lancet (London, England) 381, 680–9 (2013).
10. BeLue R et al. An overview of cardiovascular risk factor burden in sub-Saharan African
countries: a socio-cultural perspective. Global. Health 5, 10 (2009). [PubMed: 19772644]
11. Chow CK et al. Prevalence, awareness, treatment, and control of hypertension in rural and urban
communities in high-, middle-, and low-income countries. JAMA 310, 959–68 (2013).
[PubMed: 24002282]
12. Forouzanfar MH et al. Global Burden of Hypertension and Systolic Blood Pressure of at Least
110 to 115 mm Hg, 1990–2015. JAMA 317, 165–182 (2017). [PubMed: 28097354]
13. Kearney PM et al. Global burden of hypertension: analysis of worldwide data. Lancet 365,
Author Manuscript
217– 223 (2005). [PubMed: 15652604]

14. Whelton PK et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA
Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in
Adults: A Report of the American College of Cardiology/American Heart Association Task
Force on Clinical Practice Guidelines. Circulation 138, e484–e594 (2018). [PubMed: 30354654]
15. Lewington S, Clarke R, Qizilbash N, Peto R & Collins R Age-specific relevance of usual
blood pressure to vascular mortality: A meta-analysis of individual data for one million adults
in 61 prospective studies. Lancet 360, 1903–1913 (2002). [PubMed: 12493255]

16. Guo X et al. Association Between Pre-hypertension and Cardiovascular Outcomes: A

Systematic Review and Meta-analysis of Prospective Studies. Curr. Hypertens. Rep 15, 703–
Author Manuscript
716 (2013). [PubMed: 24234576]

17. SPRINT Research Group et al. A Randomized Trial of Intensive versus Standard Blood-
Pressure Control. N. Engl. J. Med 373, 2103–2116 (2015). [PubMed: 26551272]
18. Bundy JD et al. Systolic Blood Pressure Reduction and Risk of Cardiovascular Disease and
Mortality: A Systematic Review and Network Meta-analysis. JAMA Cardiol 2, 775–781
(2017). [PubMed: 28564682]
19. Bundy JD et al. Estimating the Association of the 2017 and 2014 Hypertension Guidelines With
Cardiovascular Events and Deaths in US Adults: An Analysis of National Data. JAMA Cardiol
3, 572–581 (2018). [PubMed: 29800138]
20. Wang Z et al. Status of Hypertension in China. Circulation 137, 2344–2356 (2018).
[PubMed: 29449338]
21. Muntner P et al. Measurement of Blood Pressure in Humans: A Scientific Statement From
the American Heart Association. Hypertens. (Dallas, Tex. 1979) 73, e35–e66 (2019).
22. Mills KT et al. Global Disparities of Hypertension Prevalence and Control. Circulation 134,
Author Manuscript
441– 450 (2016). [PubMed: 27502908]

23. Ataklte F et al. Burden of Undiagnosed Hypertension in Sub-Saharan Africa. Hypertension
65, 291–298 (2015). [PubMed: 25385758]
24. Martin MJ, Hulley SB, Browner WS, Kuller LH & Wentworth D Serum cholesterol, blood
pressure, and mortality: implications from a cohort of 361,662 men. Lancet (London, England) 2,
933–6 (1986).
25. Stamler J, Stamler R & Neaton JD Blood pressure, systolic and diastolic, and cardiovascular
risks. US population data. Arch. Intern. Med 153, 598–615 (1993). [PubMed: 8439223]
26. Gu D et al. Blood Pressure and Risk of Cardiovascular Disease in Chinese Men and Women.
Am. J. Hypertens 21, 265–272 (2008). [PubMed: 18188156]
27. Anderson AH et al. Time-updated systolic blood pressure and the progression of chronic
kidney disease: a cohort study. Ann. Intern. Med 162, 258–65 (2015). [PubMed: 25686166]
28. Klag MJ et al. Blood pressure and end-stage renal disease in men. N. Engl. J. Med 334, 13–18
(1996). [PubMed: 7494564]
29. Reynolds K et al. A population-based, prospective study of blood pressure and risk for end-
Author Manuscript
stage renal disease in China. J. Am. Soc. Nephrol 18, 1928–35 (2007). [PubMed: 17475822]
30. Turnbull F & Blood Pressure Lowering Treatment Trialists’ Collaboration. Effects of
different blood-pressure-lowering regimens on major cardiovascular events: results of
prospectively- designed overviews of randomised trials. Lancet (London, England) 362,
1527–35 (2003).
31. Ettehad D et al. Blood pressure lowering for prevention of cardiovascular disease and death:
a systematic review and meta-analysis. Lancet (London, England) 387, 957–967 (2016).
32. Xie X et al. Effects of intensive blood pressure lowering on cardiovascular and renal outcomes:
updated systematic review and meta-analysis. Lancet 387, 435–443 (2016). [PubMed:
26559744]
33. Cheung AK et al. Effects of Intensive BP Control in CKD. J. Am. Soc. Nephrol 28, 2812–
2823 (2017). [PubMed: 28642330]
34. Malhotra R et al. Effects of Intensive Blood Pressure Lowering on Kidney Tubule Injury in
CKD: A Longitudinal Subgroup Analysis in SPRINT. Am. J. Kidney Dis 73, 21–30 (2019).
Author Manuscript
[PubMed: 30291012]
35. Williamson JD et al. Intensive vs Standard Blood Pressure Control and Cardiovascular
Disease Outcomes in Adults Aged ≥75 Years. JAMA 315, 2673 (2016). [PubMed: 27195814]
36. ACCORD Study Group et al. Effects of intensive blood-pressure control in type 2
diabetes mellitus. N. Engl. J. Med 362, 1575–1585 (2010). [PubMed: 20228401]
37. Margolis KL et al. Outcomes of combined cardiovascular risk factor management strategies in
type 2 diabetes: the ACCORD randomized trial. Diabetes Care 37, 1721–1728 (2014). [PubMed:
24595629]
38. Kitagawa K et al. Effect of Standard vs Intensive Blood Pressure Control on the Risk of
Recurrent Stroke: A Randomized Clinical Trial and Meta-analysis. JAMA Neurol 76, 1309

(2019).

39. Singh GM et al. The age associations of blood pressure, cholesterol, and glucose: analysis of health
examination surveys from international populations. Circulation 125, 2204–2211 (2012).
Author Manuscript
[PubMed: 22492580]
40. Dorans KS, Mills KT, Liu Y & He J Trends in Prevalence and Control of Hypertension According
to the 2017 American College of Cardiology/American Heart Association (ACC/AHA)
Guideline. J. Am. Heart Assoc 7, 10.1161/JAHA.118.008888 (2018).
41. Kaufman JS, Dolman L, Rushani D & Cooper RS The contribution of genomic research to
explaining racial disparities in cardiovascular disease: a systematic review. Am. J. Epidemiol
181, 464–72 (2015). [PubMed: 25731887]
42. Whelton PK et al. Research Needs to Improve Hypertension Treatment and Control in
African Americans. Hypertension 68, 1066–1072 (2016). [PubMed: 27620388]
43. Whelton PK et al. Primary prevention of hypertension: clinical and public health advisory from
The National High Blood Pressure Education Program. Jama 288, 1882–1888 (2002). [PubMed:
12377087]
44. Powles J et al. Global, regional and national sodium intakes in 1990 and 2010: a systematic
analysis of 24 h urinary sodium excretion and dietary surveys worldwide. BMJ Open 3,
e003733 (2013).
Author Manuscript
45. National Academies of Sciences, Engineering, and Medicine, 2019. Dietary Reference Intakes
for Sodium and Potassium (2019). doi:10.17226/25353
46. He J & Whelton PK Salt intake, hypertension and risk of cardiovascular disease: an
important public health challenge. Int. J. Epidemiol 31, 322–327 (2002).
47. Elliott P et al. Intersalt revisited: further analyses of 24 hour sodium excretion and blood
pressure within and across populations. Intersalt Cooperative Research Group. BMJ 312, 1249–
1253 (1996). [PubMed: 8634612]
48. He J, Tell GS, Tang YC, Mo PS & He GQ Relation of electrolytes to blood pressure in men.
The Yi people study. Hypertens. (Dallas, Tex. 1979) 17, 378–385 (1991).
49. Mente A et al. Urinary sodium excretion, blood pressure, cardiovascular disease, and mortality:
a community-level prospective epidemiological cohort study. Lancet 392, 496–506 (2018).
[PubMed: 30129465]
50. Sacks FM et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches
to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N. Engl. J.
Author Manuscript
Med 344, 3–10 (2001). [PubMed: 11136953]

51. Midgley JP, Matthew AG, Greenwood CM & Logan AG Effect of reduced dietary sodium on
blood pressure: a meta-analysis of randomized controlled trials. JAMA (Chicago, Ill.) 275, 1590–
1597 (1996).
52. Cutler JA, Follmann D & Allender PS Randomized trials of sodium reduction: an overview. Am.
J. Clin. Nutr 65, 643S–651S (1997). [PubMed: 9022560]
53. Graudal NA, Galloe AM, Garred P, Galløe AM & Garred P Effects of sodium restriction on blood
pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride: a meta-analysis.
JAMA 279, 1383–1391 (1998). [PubMed: 9582047]
54. He FJ, Li J & MacGregor GA Effect of longer term modest salt reduction on blood pressure:
Cochrane systematic review and meta-analysis of randomised trials. BMJ 346, f1325
(2013). [PubMed: 23558162]
55. Newberry SJ et al. Sodium and Potassium Intake: Effects on Chronic Disease Outcomes and
Risks. Sodium and Potassium Intake: Effects on Chronic Disease Outcomes and Risks (Agency
for Healthcare Research and Quality (US), 2018).
Author Manuscript
56. Cook NR, Appel LJ & Whelton PK Lower levels of sodium intake and reduced cardiovascular
risk. Circulation 129, 981–989 (2014). [PubMed: 24415713]
57. He J et al. Urinary Sodium and Potassium Excretion and CKD Progression. J. Am. Soc.
Nephrol 27, 1202–1212 (2016). [PubMed: 26382905]
58. Mills KT et al. Sodium Excretion and the Risk of Cardiovascular Disease in Patients With
Chronic Kidney Disease. Jama 315, 2200–2210 (2016). [PubMed: 27218629]

59. Stolarz-Skrzypek K et al. Fatal and nonfatal outcomes, incidence of hypertension, and blood
pressure changes in relation to urinary sodium excretion. Jama 305, 1777–1785 (2011).
Author Manuscript
[PubMed: 21540421]
60. O’Donnell MJ et al. Urinary sodium and potassium excretion and risk of cardiovascular
events. Jama 306, 2229–2238 (2011). [PubMed: 22110105]
61. O’Donnell M et al. Urinary sodium and potassium excretion, mortality, and cardiovascular
events. N. Engl. J. Med 371, 612–623 (2014). [PubMed: 25119607]
62. Mente A et al. Associations of urinary sodium excretion with cardiovascular events in
individuals with and without hypertension: a pooled analysis of data from four studies. Lancet
(London, England) 388, 465–475 (2016).
63. Pfister R et al. Estimated urinary sodium excretion and risk of heart failure in men and women
in the EPIC-Norfolk study. Eur. J. Heart Fail 16, 394–402 (2014). [PubMed: 24464931]
64. Olde Engberink RHGG et al. Use of a Single Baseline Versus Multiyear 24-Hour Urine
Collection for Estimation of Long-Term Sodium Intake and Associated Cardiovascular and Renal
Risk. Circulation 136, 917–926 (2017). [PubMed: 28655835]
65. Nomura K, Asayama K, Jacobs L, Thijs L & Staessen JA Renal function in relation to sodium
Author Manuscript
intake: a quantitative review of the literature. Kidney Int 92, 67–78 (2017). [PubMed:
28412019]
66. Cobb LK et al. Methodological issues in cohort studies that relate sodium intake to
cardiovascular disease outcomes: a science advisory from the American Heart Association.
Circulation 129, 1173–1186 (2014). [PubMed: 24515991]
67. Iwahori T et al. Urinary sodium-to-potassium ratio and intake of sodium and potassium among
men and women from multiethnic general populations: the INTERSALT Study. Hypertens.
Res 42, 1590–1598 (2019). [PubMed: 30996260]
68. Weaver CM, Stone MS, Lobene AJ, Cladis DP & Hodges JK What Is the Evidence Base for
a Potassium Requirement? Nutr. Today 53, 1 (2018).
69. Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour
urinary sodium and potassium excretion. Intersalt Cooperative Research Group. BMJ 297,
319– 328 (1988). [PubMed: 3416162]
70. Cappuccio FP & MacGregor GA Does potassium supplementation lower blood pressure? A
meta- analysis of published trials. J. Hypertens 9, 465–73 (1991). [PubMed: 1649867]
Author Manuscript
71. Whelton PK et al. Effects of oral potassium on blood pressure. Meta-analysis of

randomized controlled clinical trials. JAMA 277, 1624–1632 (1997). [PubMed: 9168293]
72. Poorolajal J et al. Oral potassium supplementation for management of essential hypertension: A
meta-analysis of randomized controlled trials. PLoS One 12, e0174967 (2017). [PubMed:
28419159]
73. Filippini T, Violi F, D’Amico R & Vinceti M The effect of potassium supplementation on blood
pressure in hypertensive subjects: A systematic review and meta-analysis. Int. J. Cardiol 230,
127– 135 (2017). [PubMed: 28024910]
74. Manthey J et al. Global alcohol exposure between 1990 and 2017 and forecasts until 2030:
a modelling study. Lancet (London, England) 393, 2493–2502 (2019).
75. Klatsky AL, Friedman GD, Siegelaub AB & Gérard MJ Alcohol consumption and blood
pressure. Kaiser-Permanente Multiphasic Health Examination data. N. Engl. J. Med 296, 1194–
200 (1977). [PubMed: 854058]
76. Fuchs FD, Chambless LE, Whelton PK, Nieto FJ & Heiss G Alcohol consumption and the
Author Manuscript
incidence of hypertension: The Atherosclerosis Risk in Communities Study. Hypertens.

(Dallas, Tex. 1979) 37, 1242–50 (2001).
77. Millwood IY et al. Conventional and genetic evidence on alcohol and vascular disease aetiology:
a prospective study of 500 000 men and women in China. Lancet (London, England) 393, 1831–
1842 (2019).
78. Xin X et al. Effects of alcohol reduction on blood pressure: a meta-analysis of
randomized controlled trials. Hypertension 38, 1112–1117 (2001). [PubMed: 11711507]
79. Roerecke M et al. The effect of a reduction in alcohol consumption on blood pressure: a
systematic review and meta-analysis. Lancet Public Heal 2, e108–e120 (2017).

80. Guthold R, Stevens GA, Riley LM & Bull FC Worldwide trends in insufficient physical
activity from 2001 to 2016: a pooled analysis of 358 population-based surveys with 1·9
Author Manuscript
million participants. Lancet Glob. Heal 6, e1077–e1086 (2018).

81. Lesniak KT & Dubbert PM Exercise and hypertension. Curr. Opin. Cardiol 16, 356–9
(2001). [PubMed: 11704705]
82. Hayashi T et al. Walking to work and the risk for hypertension in men: the Osaka Health
Survey. Ann. Intern. Med 131, 21–6 (1999). [PubMed: 10391811]
83. Whelton SP, Chin A, Xin X & He J Effect of Aerobic Exercise on Blood Pressure. Ann.
Intern. Med 136, 493 (2002). [PubMed: 11926784]
84. Ishikawa K, Ohta T, Zhang J, Hashimoto S & Tanaka H Influence of age and gender on exercise
training-induced blood pressure reduction in systemic hypertension. Am. J. Cardiol 84, 192–196
(1999). [PubMed: 10426339]
85. Kelley GA & Kelley KS Progressive resistance exercise and resting blood pressure : A meta-
analysis of randomized controlled trials. Hypertens. (Dallas, Tex. 1979) 35, 838–43 (2000).
86. NCD Risk Factor Collaboration (NCD-RisC). Trends in adult body-mass index in 200
countries from 1975 to 2014: a pooled analysis of 1698 population-based measurement studies
Author Manuscript
with 19·2 million participants. Lancet 387, 1377–1396 (2016). [PubMed: 27115820]
87. Huang Z et al. Body Weight, Weight Change, and Risk for Hypertension in Women. Ann.
Intern. Med 128, 81 (1998). [PubMed: 9441586]
88. He J et al. Body mass and blood pressure in a lean population in southwestern China. Am. J.
Epidemiol 139, 380–9 (1994). [PubMed: 8109572]
89. Mertens IL & van Gaal LF Overweight, Obesity, and Blood Pressure: The Effects of
Modest Weight Reduction. Obes. Res 8, 270–278 (2000). [PubMed: 10832771]
90. Forman JP, Stampfer MJ & Curhan GC Diet and Lifestyle Risk Factors Associated With
Incident Hypertension in Women. JAMA 302, 401 (2009). [PubMed: 19622819]
91. Garrison RJ, Kannel WB, Stokes J & Castelli WP Incidence and precursors of hypertension
in young adults: the Framingham Offspring Study. Prev. Med. (Baltim) 16, 235–51 (1987).
92. Neter JE, Stam BE, Kok FJ, Grobbee DE & Geleijnse JM Influence of weight reduction on
blood pressure: a meta-analysis of randomized controlled trials. Hypertension 42, 878–884
(2003). [PubMed: 12975389]
93. Whelton SP et al. Effect of dietary fiber intake on blood pressure: a meta-analysis of
Author Manuscript
randomized, controlled clinical trials. J. Hypertens 23, 475–481 (2005). [PubMed: 15716684]
94. Streppel MT, Arends LR, van ‘t Veer P, Grobbee DE & Geleijnse JM Dietary fiber and blood
pressure: a meta-analysis of randomized placebo-controlled trials. Arch. Intern. Med 165, 150–6
(2005). [PubMed: 15668359]
95. Liu L, Ikeda K, Sullivan DH, Ling W & Yamori Y Epidemiological evidence of the association
between dietary protein intake and blood pressure: a meta-analysis of published data. Hypertens.
Res 25, 689–95 (2002). [PubMed: 12452320]
96. Rebholz CM et al. Dietary Protein Intake and Blood Pressure: A Meta-Analysis of
Randomized Controlled Trials. Am. J. Epidemiol 176, S27–S43 (2012). [PubMed: 23035142]
97. Margetts BM, Beilin LJ, Armstrong BK, Vandongen R & Croft KD Dietary fat intake and
blood pressure: a double blind controlled trial of changing polyunsaturated to saturated fat
ratio. J. Hypertens. Suppl 2, S201–3 (1984). [PubMed: 6400366]
98. Puska P et al. Controlled, randomised trial of the effect of dietary fat on blood pressure.
Lancet (London, England) 1, 1–5 (1983).
Author Manuscript
99. Imamura F et al. Dietary quality among men and women in 187 countries in 1990 and 2010:
a systematic assessment. Lancet. Glob. Heal 3, e132–42 (2015).
100. Appel LJ et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH
Collaborative Research Group. N. Engl. J. Med 336, 1117–1124 (1997). [PubMed:
9099655]
101. Yokoyama Y et al. Vegetarian Diets and Blood Pressure. JAMA Intern. Med 174, 577
(2014). [PubMed: 24566947]
102. Nordmann AJ et al. Meta-Analysis Comparing Mediterranean to Low-Fat Diets for
Modification of Cardiovascular Risk Factors. Am. J. Med 124, 841–851.e2 (2011). [PubMed:
21854893]

103. Baer L & Radichevich I Cigarette smoking in hypertensive patients. Blood pressure and
endocrine responses. Am. J. Med 78, 564–568 (1985). [PubMed: 2984931]
Author Manuscript
104. Rhee M-Y, Na S-H, Kim Y-K, Lee M-M & Kim H-Y Acute effects of cigarette smoking on
arterial stiffness and blood pressure in male smokers with hypertension. Am. J. Hypertens
20, 637–41 (2007). [PubMed: 17531920]
105. Wang Y et al. Relationship between Duration of Sleep and Hypertension in Adults: A
Meta- Analysis. J. Clin. Sleep Med 11, 1047–56 (2015). [PubMed: 25902823]
106. Bazzano LA, Khan Z, Reynolds K & He J Effect of Nocturnal Nasal Continuous Positive
Airway Pressure on Blood Pressure in Obstructive Sleep Apnea. Hypertension 50, 417–423
(2007). [PubMed: 17548722]
107. Virdis A, Giannarelli C, Fritsch Neves M, Taddei S & Ghiadoni L Cigarette Smoking
and Hypertension. Curr. Pharm. Des 16, 2518–2525 (2010). [PubMed: 20550499]
108. Halperin RO, Michael Gaziano J & Sesso HD Smoking and the Risk of Incident Hypertension
in Middle-aged and Older Men. Am. J. Hypertens 21, 148–152 (2008). [PubMed: 18174885]
109. Cai Y et al. Associations of Short-Term and Long-Term Exposure to Ambient Air Pollutants
With Hypertension. Hypertension 68, 62–70 (2016). [PubMed: 27245182]
Author Manuscript
110. Yang B-Y et al. Global association between ambient air pollution and blood pressure: A
systematic review and meta-analysis. Environ. Pollut 235, 576–588 (2018). [PubMed:
29331891]
111. Liu M-Y, Li N, Li WA & Khan H Association between psychosocial stress and hypertension:
a systematic review and meta-analysis. Neurol. Res 39, 573–580 (2017). [PubMed:
28415916]
112. Manohar S, Thongprayoon C, Cheungpasitporn W, Mao MA & Herrmann SM Associations
of rotational shift work and night shift status with hypertension: a systematic review and
meta- analysis. J. Hypertens 35, 1929–1937 (2017). [PubMed: 28650914]
113. van Kempen E, Casas M, Pershagen G & Foraster M WHO Environmental Noise Guidelines
for the European Region: A Systematic Review on Environmental Noise and Cardiovascular
and Metabolic Effects: A Summary. Int. J. Environ. Res. Public Health 15, 379 (2018).
114. Dzhambov AM & Dimitrova DD Residential road traffic noise as a risk factor for hypertension
in adults: Systematic review and meta-analysis of analytic studies published in the period 2011–
2017. Environ. Pollut 240, 306–318 (2018). [PubMed: 29751327]
Author Manuscript
115. Bowman TS, Gaziano JM, Buring JE & Sesso HD A prospective study of cigarette smoking
and risk of incident hypertension in women. J. Am. Coll. Cardiol 50, 2085–92 (2007).
[PubMed: 18021879]
116. Gerace TA, Hollis J, Ockene JK & Svendsen K Smoking cessation and change in diastolic blood
pressure, body weight, and plasma lipids. MRFIT Research Group. Prev. Med. (Baltim) 20,
602– 20 (1991).
117. Huang K et al. Long-Term Exposure to Fine Particulate Matter and Hypertension Incidence
in China. Hypertension 73, 1195–1201 (2019). [PubMed: 31067193]
118. Yusuf S et al. Modifiable risk factors, cardiovascular disease, and mortality in 155 722
individuals from 21 high-income, middle-income, and low-income countries (PURE): a
prospective cohort study. Lancet (2019). doi:10.1016/S0140-6736(19)32008-2
119. Nagele E et al. Clinical effectiveness of stress-reduction techniques in patients with
hypertension: systematic review and meta-analysis. J. Hypertens 32, 1936–44; discussion 1944
(2014). [PubMed: 25084308]
Author Manuscript
120. Whelton PK et al. Sodium reduction and weight loss in the treatment of hypertension in older
persons: a randomized controlled trial of nonpharmacologic interventions in the elderly
(TONE). TONE Collaborative Research Group. Jama 279, 839–846 (1998). [PubMed: 9515998]
121. Cook NR et al. Long term effects of dietary sodium reduction on cardiovascular disease
outcomes: observational follow-up of the trials of hypertension prevention (TOHP). BMJ
334, 885–888 (2007). [PubMed: 17449506]
122. Beaney T et al. May Measurement Month 2017: an analysis of blood pressure screening
results worldwide. Lancet Glob. Heal 6, e736–e743 (2018).
123. Borzecki AM, Oliveria SA & Berlowitz DR Barriers to hypertension control. Am. Heart J
149, 785–794 (2005). [PubMed: 15894958]

124. Khatib R et al. Patient and healthcare provider barriers to hypertension awareness, treatment
and follow up: a systematic review and meta-analysis of qualitative and quantitative studies.
Author Manuscript
PLoS One 9, e84238 (2014). [PubMed: 24454721]

125. Mills KT et al. Comparative effectiveness of implementation strategies for blood pressure
control in hypertensive patients: A systematic review and meta-analysis. Ann. Intern. Med 168,
110–120 (2018). [PubMed: 29277852]
126. He J et al. Effect of a Community Health Worker-Led Multicomponent Intervention on Blood
Pressure Control in Low-Income Patients in Argentina: A Randomized Clinical Trial. JAMA
318, 1016–1025 (2017). [PubMed: 28975305]
127. Piper MA et al. Diagnostic and Predictive Accuracy of Blood Pressure Screening Methods
With Consideration of Rescreening Intervals: A Systematic Review for the U.S. Preventive
Services Task Force. Ann. Intern. Med 162, 192 (2015). [PubMed: 25531400]
128. Yang W-Y et al. Association of Office and Ambulatory Blood Pressure With Mortality
and Cardiovascular Outcomes. JAMA 322, 409 (2019). [PubMed: 31386134]
129. Siu AL Screening for High Blood Pressure in Adults: U.S. Preventive Services Task
Force Recommendation Statement. Ann. Intern. Med 163, 778 (2015). [PubMed:
26458123]
Author Manuscript
130. Agarwal R, Bills JE, Hecht TJW & Light RP Role of Home Blood Pressure Monitoring in
Overcoming Therapeutic Inertia and Improving Hypertension Control. Hypertension 57, 29–
38 (2011). [PubMed: 21115879]
131. Olsen MH et al. A call to action and a lifecourse strategy to address the global burden of
raised blood pressure on current and future generations: the Lancet Commission on
hypertension. Lancet (London, England) 388, 2665–2712 (2016).
132. Bao W, Threefoot SA, Srinivasan SR & Berenson GS Essential hypertension predicted by
tracking of elevated blood pressure from childhood to adulthood: the Bogalusa Heart Study.
Am. J. Hypertens 8, 657–65 (1995). [PubMed: 7546488]
133. Zhang T et al. Trajectories of Childhood Blood Pressure and Adult Left Ventricular
Hypertrophy. Hypertension 72, 93–101 (2018). [PubMed: 29785961]
134. Li S, Chen W, Srinivasan SR & Berenson GS Childhood Blood Pressure as a Predictor of
Arterial Stiffness in Young Adults. Hypertension 43, 541–546 (2004). [PubMed: 14744922]
135. Gaziano TA, Bitton A, Anand S, Weinstein MC & International Society of Hypertension.
Author Manuscript
The global cost of nonoptimal blood pressure. J. Hypertens 27, 1472–1477 (2009).
[PubMed: 19474763]
136. Kirkland EB et al. Trends in Healthcare Expenditures Among US Adults With
Hypertension: National Estimates, 2003–2014. J. Am. Heart Assoc 7, (2018).
137. Zhang D, Wang G, Zhang P, Fang J & Ayala C Medical Expenditures Associated With
Hypertension in the U.S., 2000–2013. Am. J. Prev. Med 53, S164–S171 (2017).
[PubMed: 29153117]
138. Wang G, Fang J & Ayala C Hypertension-associated hospitalizations and costs in the
United States, 1979–2006. Blood Press 23, 126–33 (2014). [PubMed: 23885763]
139. Wang G, Yan L, Ayala C, George MG & Fang J Hypertension-associated expenditures for
medication among US adults. Am. J. Hypertens 26, 1295–302 (2013). [PubMed: 23727748]
140. Heidenreich PA et al. Forecasting the Future of Cardiovascular Disease in the United
States. Circulation 123, 933–944 (2011). [PubMed: 21262990]
141. Nakamura K et al. Treated and untreated hypertension, hospitalization, and medical
Author Manuscript
expenditure: an epidemiological study in 314622 beneficiaries of the medical insurance system

in Japan. J. Hypertens 31, 1032–42 (2013). [PubMed: 23449017]
142. ARREDONDO A & ZUNIGA A Epidemiologic Changes and Economic Burden of Hypertension
in Latin AmericaEvidence from Mexico. Am. J. Hypertens 19, 553–559 (2006). [PubMed:
16733225]
143. Arredondo A & Aviles R Hypertension and Its Effects on the Economy of the Health System
for Patients and Society: Suggestions for Developing Countries. Am. J. Hypertens 27, 635–636
(2014). [PubMed: 24610899]
144. Global Burden of Disease Health Financing Collaborator Network, A. Y. et al. Past, present, and
future of global health financing: a review of development assistance, government, out-of-
pocket,

and other private spending on health for 195 countries, 1995–2050. Lancet (London, England)
393, 2233–2260 (2019).
Author Manuscript
145. Woolf SH A closer look at the economic argument for disease prevention. JAMA 301, 536–
8 (2009). [PubMed: 19190319]
146. Park M et al. Associations between kidney function and subclinical cardiac abnormalities
in CKD. J. Am. Soc. Nephrol 23, 1725–1734 (2012). [PubMed: 22935481]
147. Bress AP et al. Cost-Effectiveness of Intensive versus Standard Blood-Pressure Control. N.
Engl. J. Med 377, 745–755 (2017). [PubMed: 28834469]
148. Gu D et al. The Cost-Effectiveness of Low-Cost Essential Antihypertensive Medicines for
Hypertension Control in China: A Modelling Study. PLoS Med 12, e1001860 (2015).
[PubMed: 26241895]
149. Lakdawalla DN et al. Defining Elements of Value in Health Care-A Health Economics
Approach: An ISPOR Special Task Force Report [3]. Value Health 21, 131–139 (2018).
[PubMed: 29477390]
150. Marzorati C & Pravettoni G Value as the key concept in the health care system: how it has
influenced medical practice and clinical decision-making processes. J. Multidiscip. Healthc 10,
Author Manuscript
101–106 (2017). [PubMed: 28356752]

151. GBD 2013 DALYs and HALE Collaborators, C. J. L. et al. Global, regional, and national
disability-adjusted life years (DALYs) for 306 diseases and injuries and healthy life
expectancy (HALE) for 188 countries, 1990–2013: quantifying the epidemiological transition.
Lancet (London, England) 386, 2145–91 (2015).
152. Blacher J, Levy BI, Mourad J-J, Safar ME & Bakris G From epidemiological transition to
modern cardiovascular epidemiology: hypertension in the 21st century. Lancet (London,
England) 388, 530–2 (2016).
153. He J et al. Major Causes of Death among Men and Women in China. N. Engl. J. Med 353,
1124– 1134 (2005). [PubMed: 16162883]
154. Bi Y et al. Status of Cardiovascular Health in Chinese Adults. J. Am. Coll. Cardiol 65,
1013– 1025 (2015). [PubMed: 25766949]
155. Yang W et al. Prevalence of Diabetes among Men and Women in China. N. Engl. J. Med
362, 1090–1101 (2010). [PubMed: 20335585]
Author Manuscript
Author Manuscript

KEY POINTS
Author Manuscript
leading modifiable risk factor for cardiovascular disease and premature death worldwide.
•
absolute burden of hypertension is rising globally, especially in low and middle-income countries (LMICs).
nt, and control of hypertension are unacceptably low worldwide, particularly in LMICs.
•
actors, including high sodium intake, low potassium intake, obesity, alcohol consumption, physical inactivity and unhealthy diet, are recommended for th
mentation strategies for hypertension prevention and control are needed to address barriers at the patient, provider, system, and community levels.
essments are needed to evaluate the economic• impact of hypertension worldwide.
•
Author Manuscript
•
Author Manuscript
Author Manuscript

Author Manuscript
Author Manuscript
Figure 1. Changes in mean estimated blood pressure by world region between 1975 and 2015.
A. Change in systolic blood pressure (BP) in men. B. Change in systolic BP in women.
C. Change in diastolic BP in men. D. Change in diastolic BP in Women. Data obtained
from reference4.
Author Manuscript
Author Manuscript

Author Manuscript
Author Manuscript
Author Manuscript
Figure 2. Hypertension prevalence by world region in 2010.

Prevalence of hypertension defined as systolic BP ≥140 mmHg or diastolic BP ≥90
mmHg or use of antihypertensive medication in A. Men and B. Women. Data obtained
from reference3.
Author Manuscript

Author Manuscript
Author Manuscript
Author Manuscript
Figure 3. Causes of deaths worldwide attributed to increased blood pressure in 2015.

A. Estimated numbers of deaths attributed to systolic blood pressure (SBP) ≥110–115
mmHg and B. SBP ≥140 mmHg by cause of death. Data obtained from reference12.
Author Manuscript

Table 1.
Estimated prevalence of hypertension in high-income and low and middle-income countries in 2000 and 2010
Mills et al.
Population 2000 2010
Men Women Men Women
Age-standardized prevalence % (95% CIs)
Global 26.4 (24.6–28.2) 25.1 (23.4–26.9) 31.9 (30.3–33.5) 30.1 (28.5–31.6)
High-income countries 35.1 (29.8–40.3) 26.9 (22.6–31.3) 31.6 (29.6–33.6) 25.3 (23.9–26.7)
27.
Low and middle-income countries 23.4 (21.6–25.2) 24.1 (22.4–25.9) 31.7 (29.7–33.6) 31.2 (29.3–33.1)
Absolute numbers in millions (95% CIs)
Global 457.0 (422.9, 491.2) 464.1 (432.0, 496.2) 694.4 (658.7–730.1) 693.5 (659.5–727.5)
Low- and middle-income countries 294.3 (268.2–320.3) 304.6 (280.5–328.8) 520.1 (485.6–554.7) 518.8 (485.7–552.0)
Data obtained from reference3
Page 32
Table 2.
Estimated prevalence of hypertension in the general populations of the US in 2013–2016 and China in 2012–2015
Mills et al.
Population Age-standardized prevalence of hypertension (% (95% CI)
Blood pressure ≥140/90 mmHg* Blood pressure ≥130/80 mmHg†

US 2013–2016 Men 32.1 (30.2–34.0) 48.0 (45.7–50.3)
Women 31.8 (29.8–33.8) 43.1 (41.3–44.9)
Total 32.0 (30.3–33.6) 45.4 (43.9–46.9)
27.
China 2012–2015 Men 24.5 (23.0–26.0) 52.3 (50.0–54.5)

Women 21.9 (20.7–23.1) 40.4 (38.0–42.9)
Total 23.2 (21.9–24.5) 46.4 (44.2–48.7)
*
Systolic blood pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg and/or use of antihypertensive medications.
†
Systolic blood pressure ≥130 mm Hg and/or diastolic blood pressure ≥80 mm Hg and/or use of antihypertensive
medications. Data obtained from references 19 and 20
Page 33
Table 3.
Hypertension control in high income and low and middle income countries in 2000 and 2010
Mills et al.
2000 2010
Population
Men Women Men Women
Age-standardized proportion of hypertension control in all patients with hypertension (% (95% CI))
Global 10.0 (4.0–15.9) 13.4 (6.5–20.2) 10.9 (7.7–14.2) 16.8 (13.1–20.5)
27.
Age-standardized proportion of hypertension control in patients with treated hypertension (% (95% CI))
Global 34.2 (24.1–44.2) 33.7 (23.2–44.2) 35.8 (30.8–40.7) 38.0 (33.2–42.8)
Data obtained from reference3
Page 34

JURNALL

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

JURNALL

Uploaded by

Copyright:

Available Formats

HHS Public Access

Published in final edited form as:

The global epidemiology of hypertension

rapidly increasing burden of hypertension and BP-related cardiovascular diseases, in

GLOBAL MEAN BLOOD PRESSURE

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

GLOBAL BURDEN OF HYPERTENSION

contrast, HICs experienced a decrease in hypertension prevalence from 31.1% to 28.5% in

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

In 2017, the American College of Cardiology/American Heart Association Task Force on

appropriate BP cuff sizes, and preparation of participants), and number of BP measurements

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

BLOOD PRESSURE, CVD, CKD AND MORTALITY

hemorrhagic stroke deaths).12 Consistent with trends in hypertension prevalence, the

Observational epidemiological studies have shown a strong, independent and linear

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

meta-regression methods by enabling the simultaneous comparison of the effects of

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

In addition, a meta-analysis of four randomized clinical trials with 4,895 participants

RISK FACTORS FOR HYPERTENSION

High sodium intake

Animal experiments, observational epidemiologic studies, and randomized clinical trials

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

intermediate to a lower level resulted in an additional reduction in systolic BP of 4.6 mmHg

Low potassium intake

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

Randomized clinical trials have shown that potassium supplementation lowers BP in

Alcohol consumption—Globally, alcohol consumption varies considerably, with the

Risk in Communities Study reported a J-shaped association between alcohol consumption

A meta-analysis of 15 randomized control trials with a total of 2,234 participants reported

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

These findings suggest that reducing alcohol intake should be recommended as an

Lack of physical activity

much higher in urbanized populations in high-income countries.80

Epidemiological studies have reported an inverse relationship between physical activity,

is an effective lifestyle intervention for the prevention and treatment of hypertension.

Overweight and obesity

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

90,91In a meta-analysis of 25 randomized controlled trials with 4,874 participants, a net

vegetables.102 A meta-analysis of 6 trials with a total of 2,650 participants reported a modest

1.5 mmHg (95% CI 0.8–2.1) in Mediterranean diets compared to low-fat diets.102

Other potential risk factors

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

effects of different stress-reduction techniques, such as biofeedback, relaxation or combined

4.31) and diastolic BP by 1.83 mm Hg (95% CI 0.61–3.05) in a meta-analysis of 16

In summary, observational studies have reported weak or moderate associations between

HYPERTENSION CONTROL IN THE COMMUNITY

Large-scale screening programs in communities or health facilities could be an effective

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

Barriers to hypertension control exist at multiple levels: patients, healthcare providers,

Most trials of implementation strategies to overcome barriers to BP control have been

Increased use of out-of-office BP measurements for confirmation of hypertension diagnosis

measurements (ABPM) predicted long-term CVD outcomes independently of office BP

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

The prevention and control of hypertension in communities requires a life-course approach.

THE FINANCIAL BURDEN OF HYPERTENSION

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

Medical Expenditure Panel Survey which used self-reported history of hypertension to

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

minority populations in HICs.42 To accurately estimate the global burden of hypertension,

Nat Rev Nephrol. Author manuscript; available in PMC 2021 March

to accurately assess the financial burden of hypertension worldwide.

Regression dilution (bias)